No abstract

Non-technical summary Non-invasive neuromodulation of the human brain -with pulsed magnetic fields or small direct currents -is becoming increasingly popular for treating a variety of neurological and neuropsychiatric disorders. In the present work we investigated in healthy humans the possibility of a non-invasive modulation of motor cortex excitability by the application of static magnetic fields through the scalp. We found that transcranial static magnetic field stimulation (tSMS) can reduce the excitability of the motor cortex for a period that outlasts the time of the application of the magnetic field. Moreover, we demonstrated that these excitability changes take origin at the cortical level. These results suggest that tSMS using small static magnets may be a promising tool to modulate cerebral excitability in a non-invasive, painless and reversible way.Abstract The aim of the present study was to investigate in healthy humans the possibility of a non-invasive modulation of motor cortex excitability by the application of static magnetic fields through the scalp. Static magnetic fields were obtained by using cylindrical NdFeB magnets. We performed four sets of experiments. In Experiment 1, we recorded motor potentials evoked by single-pulse transcranial magnetic stimulation (TMS) of the motor cortex before and after 10 min of transcranial static magnetic field stimulation (tSMS) in conscious subjects. We observed an average reduction of motor cortex excitability of up to 25%, as revealed by TMS, which lasted for several minutes after the end of tSMS, and was dose dependent (intensity of the magnetic field) but not polarity dependent. In Experiment 2, we confirmed the reduction of motor cortex excitability induced by tSMS using a double-blind sham-controlled design. In Experiment 3, we investigated the duration of tSMS that was necessary to modulate motor cortex excitability. We found that 10 min of tSMS (compared to 1 min and 5 min) were necessary to induce significant effects. In Experiment 4, we used transcranial electric stimulation (TES) to establish that the tSMS-induced reduction of motor cortex excitability was not due to corticospinal axon and/or spinal excitability, but specifically involved intracortical networks. These results suggest that tSMS using small static magnets may be a promising tool to modulate cerebral excitability in a non-invasive, painless, and reversible way.

Non-local methods for image denoising and inpainting have gained considerable attention in recent years. This is in part due to their superior performance in textured images, a known weakness of purely local methods. Local methods on the other hand have demonstrated to be very appropriate for the recovering of geometric structures such as image edges. The synthesis of both types of methods is a trend in current research. Variational analysis in particular is an appropriate tool for a unified treatment of local and nonlocal methods. In this work we propose a general variational framework for non-local image inpainting, from which important and representative previous inpainting schemes can be derived, in addition to leading to novel ones. We explicitly study some of these, relating them to previous work and showing results on synthetic and real images.

This study has focused on how sensory stimulation affects gait in Parkinson's disease (PD). The kinematic parameters of gait [cadence, step amplitude, velocity, coefficient of variation of stride time (CV(stride-time)), and the coefficient of variation of the step amplitude (CV(step-amplitude))] were analysed in 25 PD patients and 10 control subjects. Step amplitude, velocity and CV(stride-time) were altered in the patients with PD. However, when kinematic parameters were analysed as a function of disease severity, none of the parameters differed between early PD (I-II Hoehn and Yahr) and the controls. Nevertheless, more severely affected PD patients (III-IV Hoehn and Yahr) walked with a reduced step amplitude, lower velocity, higher CV(stride-time), and higher CV(step-amplitude) than the controls. The administration of auditory stimulation at a frequency matching the preferred walking cadence led to a decrease in the CV(stride-time) in PD(III-IV) patients, and to an increase in step amplitude in PD(III-IV )and controls. Visual stimulation at the same frequency did not modify any of the altered kinematic parameters in PD(III-IV )patients. When different stimulation frequencies were utilised, auditory stimulation significantly changed some of the altered walking parameters in Parkinson patients. Frequencies matching preferred walking cadence or above this, up to the fastest walking, were those that seem to interact most effectively with the abnormal kinematic parameters in PD(III-IV )patients. Visual stimulation negatively modulated cadence in PD(III-IV) in the frequency range used. Sensory stimulation facilitates gait in PD. Studies using sensory stimulation as a tool to facilitate walking should take into account the grade of disability of the patients.

Freezing of gait (FOG) in Parkinson's disease (PD) rises in prevalence when the effect of medications decays. It is known that auditory rhythmic stimulation improves gait in patients without FOG (PD-FOG), but its putative effect on patients with FOG (PD+FOG) at the end of dose has not been evaluated yet. This work evaluates the effect of auditory rhythmic stimulation on PD+FOG at the end of dose. 10 PD+FOG and 9 PD-FOG patients both at the end of dose periods, and 10 healthy controls were asked to perform several walking tasks. Tasks were performed in the presence and absence of auditory sensory stimulation. All PD+FOG suffered FOG during the task. The presence of auditory rhythmic stimulation (10% above preferred walking cadence) led PD+FOG to significantly reduce FOG. Velocity and cadence were increased, and turn time reduced in all groups. We conclude that auditory stimulation at the frequency proposed may be useful to avoid freezing episodes in PD+FOG.